This SuperSeries is composed of the SubSeries listed below.
TCF7L2 is a master regulator of insulin production and processing.
Sex, Age, Specimen part
View SamplesHere we harnessed the potential of expression arrays in 89 human pancreatic islet donors (different levels of blood glucose (HbA1c)) to identify genes regulated in this relevant tissue for type 2 diabetes (T2D).
TCF7L2 is a master regulator of insulin production and processing.
Sex, Age, Specimen part
View SamplesClose to 50 genetic loci have been associated with type 2 diabetes (T2D), but they explain only 15% of the heritability.
A systems genetics approach identifies genes and pathways for type 2 diabetes in human islets.
Sex, Age, Specimen part
View SamplesExpression profiling of cell cycle genes in human pancreatic islets with and without type 2 diabetes
Autoimmunity against INS-IGF2 protein expressed in human pancreatic islets.
Sex, Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Identification and validation of single-sample breast cancer radiosensitivity gene expression predictors.
No sample metadata fields
View SamplesIn this study gene expression profiles for 307 cases of advanced bladder cancers were compared to molecular phenotype at the tumor cell level. TUR-B tissue for RNA extraction was macrodissected from the close vicinity of the tissue sampled for immunohistochemistry to ensure high-quality sampling and to minimize the effects of intra-tumor heterogeneity. Despite excellent agreement between gene expression values and IHC-score at the single marker level, broad differences emerge when samples are clustered at the global mRNA versus tumor cell (IHC) levels. Classification at the different levels give different results in a systematic fashion, which implicates that analysis at both levels is required for optimal subtype-classification of bladder cancer.
Molecular classification of urothelial carcinoma: global mRNA classification versus tumour-cell phenotype classification.
Specimen part
View SamplesPurpose
Identification and validation of single-sample breast cancer radiosensitivity gene expression predictors.
No sample metadata fields
View SamplesPancreatic islets are central in type 2-diabetes development, which coincides with increased activity of innate immunity. Intriguingly, human pancreatic islets express many complement genes. The most highly expressed gene was the complement inhibitor CD59 that is GPI anchored to the cell membrane, which unexpectedly was found in high amounts intracellularly in beta cells. Silencing of CD59 strongly suppressed insulin secretion. Importantly, this suppression was unrelated to established CD59 functions, but rather depletion of intracellular CD59. Imaging experiments identified a distal site of inhibition in the exocytotic pathway, but prior to emptying of the insulin granules. Proximity Ligation Assays pin-pointed the mechanism to impaired turnover of exocytosis-regulating SNARE-proteins and CD59 was detected in complex with VAMP2 and syntaxin. CD59 was downregulated by 24-h glucose incubations in human islets, rat cell lines and in islets from three rodent diabetes models.
The complement inhibitor CD59 regulates insulin secretion by modulating exocytotic events.
Specimen part
View SamplesThis SuperSeries is composed of the SCANB SubSeries listed below.
The Sweden Cancerome Analysis Network - Breast (SCAN-B) Initiative: a large-scale multicenter infrastructure towards implementation of breast cancer genomic analyses in the clinical routine.
Specimen part
View SamplesHuman brown fat tumors (hibernomas) display concomitant loss of the tumor suppressor genes MEN1 and AIP. In the present study, we hypothesized that the brown fat phenotype is attributed to these mutations. Accordingly, we demonstrate that silencing of AIP in human brown preadipocytic and white fat cell lines results in the induction of the brown fat marker UCP1. In human adipocytic tumors, loss of MEN1 was found both in white (one out of 51 lipomas) and brown fat tumors. In contrast, concurrent loss of AIP was always accompanied by a brown fat morphology. We conclude that this white-to-brown phenotype switch in brown fat tumors is mediated by the loss of AIP.
Loss of the tumour suppressor gene AIP mediates the browning of human brown fat tumours.
Specimen part
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